Obesity and asthma are associated conditions, with asthma incidence almost doubled in obese compared with healthy weight individuals. Obese asthmatics experience more severe asthma symptoms, poorer lung function and a reduced quality of life compared with asthmatics of a healthy weight. Furthermore, they do not respond well to inhaled corticosteroid medications; the mainstay of asthma pharmacotherapy. The mechanisms responsible for this association are not understood. A number of hypotheses have been proposed including inflammation, gastro-oesophageal reflux and mechanical factors. Asthma is an inflammatory condition of the airways, in which both eosinophilic and noneosinophilic patterns of inflammation have been described. Noneosinophilic asthma is characterised by an increase in airway neutrophils, airway hyperresponsiveness and activation of the innate immune response. Obesity is also an inflammatory condition, as the presence of excess adipose tissue leads to chronic low-grade inflammation. A high dietary fat intake is often associated with obesity and may also contribute to inflammation in obesity, as saturated fatty acids stimulate innate immune pathways. It is plausible that this activation of the innate immune response extends to the airways of susceptible individuals, leading to increased levels of airway neutrophils. Neutrophils are of importance in asthma because elevated levels in the airways are associated with the most severe forms of asthma and negatively correlate with airflow obstruction. In Chapter 3 of this thesis, we examined the association between obesity and airway inflammation in subjects with asthma. There was a significant association between body mass index and airway neutrophils in females with asthma. In asthmatic males, saturated fatty acids were associated with increased neutrophilic airway inflammation. These observations suggest that both obesity and saturated fat may independently activate innate immune responses, leading to a more neutrophilic pattern of airway inflammation, with distinct differences between males and females. In Chapter 4, the relationship between body composition, lung function and inflammation is investigated. Previous research has shown that increased adiposity within the android and thoracic regions is associated with respiratory function impairment. This thesis suggests that these influences are sexually dimorphic in nature. Android and upper body adiposity were negatively associated with lung function in females, whilst android lean mass was an important positive predictor of lung function in males. In Chapters 5 and 6, the effect of dietary restriction and/or increased physical activity on weight loss and asthma outcomes is explored. This pilot study found that both caloric restriction and increased physical activity are not only feasible and efficacious weight loss strategies in asthma, but also lead to improved quality of life and asthma control. Importantly, a decrease in neutrophilic airway inflammation correlated with adipose tissue reduction in females, and dietary fat in males, supporting our observations in Chapter 3, that these factors contribute to the obese-asthma phenotype. Also in Chapter 6, we describe a relationship between increased physical activity and reduced airway eosinophilia. Obese adults are 50% less likely to participate in sufficient physical activity compared to those within the healthy weight range. Therefore, it is plausible that physical inactivity is a driver of the obese-asthma phenotype. This thesis indicates that increased exercise is associated with reduced eosinophilic airway inflammation in overweight and obese individuals with asthma. The aetiology of obesity is multifactorial, often involving an elevated dietary fat intake, low level of exercise and ultimately an excess of adipose tissue. This thesis suggests that these aetiologies are also independently involved in the development of the obese-asthma phenotype. This phenotype involves both innate and adaptive immune responses, and mechanical effects of excess adipose tissue. Importantly these inflammatory pathways are reversible, which suggests that the obese-asthma phenotype is also reversible. The data presented in this thesis suggests several mechanisms by which dietary intake and physical activity modulate the expression of obese-asthma. Further work is this area will enable management strategies to be developed for this large and increasingly prevalent asthma phenotype.